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Apoptosis in Gingival Overgrowth Tissues

¹ Department of Periodontology and Oral Biology, Boston University, Goldman School of Dental Medicine, 700 Albany Street W-210, Boston, MA 02118, USA;
² Department of Periodontology, Dental Clinic, St. Ann’s Teaching Hospital, Pekarska 53, 656 91 Brno, Czech Republic;
³ Department of Periodontology, Istanbul University, Faculty of Dentistry, Istanbul, Turkey;
⁴ Franciscan Hospital for Children, Boston, MA, USA; and
⁵ Department of Biochemistry, Boston University, School of Medicine, Boston, MA, USA

^* corresponding author, trackman{at}bu.edu

Variations in the balance between cell proliferation and apoptosis could contribute to the etiology of gingival overgrowth. The aim of this study was to test the hypothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is decreased. Apoptotic index, caspase 3 expression, the proliferative index, FOXO1 expression, and histological inflammation were measured in situ. Analysis of data showed that apoptosis decreased in all forms of gingival overgrowth examined (p < 0.05), and inflammation caused a small but significant increase compared with non-inflamed tissues (p < 0.05). The greatest decrease of apoptosis occurred in the most fibrotic tissues. Cell proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation (p < 0.05). To identify potential mechanisms of transcriptional regulation of apoptosis, we assessed FOXO1 and caspase 3 expression levels and found them to correlate well with diminished apoptosis. Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in apoptosis contribute to gingival overgrowth.

KEY WORDS: gingival overgrowth • fibrosis • fibroblast • apoptosis • FOXO1